Chronic immune thrombocytopenic purpura (ITP) is an autoimmune disorder characterized by thrombocytopenia due to the production of antiplatelet autoantibodies which result in platelet destruction by the reticuloendothelial system or inhibition of platelet production (McMillan, NEJM 304: 1135-1147 (1981); Kelton, et al., Semin. Thromb. Haemost. 8: 83-104 (1982). Autoantibody from approximately three-fourths of these patients is known to react with the membrane glycoprotein (GP) complexes --GPIIb/IIIa or GPIb/IX van Leeuwen, et al., Blood 59: 23-26 (1982); Woods, et al., Blood 63: 368-375 (1984); Woods, et al., Blood 64: 156-160 (1984); Beardsley, et al., J. Clin. Invest. 74: 1701-1707; and McMillan, et al., Blood 70: 1040-1045 (1987); of these, some have been shown to bind to GPIIIa Beardsley, et al., Id. However, little information is available on the precise location of epitopes on GPIIIa. A recent abstract by Kekomaki et al. showed that plasma from one ITP patient, which reacted with GPIIIa by immunoblotting, bound to a 60,000 dalton GPIIIa fragment resulting from chymotrypsin digestion Blood 74: 91 (1989).